Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 216, Issue 1-2, Pages 118-121Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2009.07.008
Keywords
Microglia; Macrophages; Respiratory burst; Reactive oxygen species; Ion channels
Categories
Funding
- German Research Foundation [SFB 507/C7]
- St. George's, University of London
- Wellcome Trust
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Activated microglial cells generate reactive oxygen species (ROS), which have detrimental effects in neuroinflammatory and neurodegenerative diseases. In the present study, we have identified a novel mechanism involved in microglial NADPH oxidase-mediated ROS production. In PMA-stimulated microglia, ROS production was substantially reduced upon inhibition of the non-selective cation channel TRPV1 with La3+, ruthenium red, capsazepine and 5-iodo-resinferatoxin. Furthermore, sustained membrane depolarization, a hallmark of NADPH oxidase activity in phagocytes, was found to induce non-selective cation/TRPV1 channel activity in microglia. Together, our data suggest that TRPV1 channels are involved in regulating NADPH oxidase-mediated ROS generation in microglia. (C) 2009 Elsevier B.V. All rights reserved.
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